ライフサイエンスコーパス: tubular epithelial cell

1 by stimulating apoptosis in endothelial and tubular epithelial cell.

2 Hypoxia significantly increased HE4 in renal tubular epithelial cells.

3 in primary neuronal cells and renal proximal tubular epithelial cells.

4 expression, and internalization within renal tubular epithelial cells.

5 d an enrichment of miR-24 in endothelial and tubular epithelial cells.

6 and by inhibiting bacteria invasion of renal tubular epithelial cells.

7 t decrease in proliferation and apoptosis of tubular epithelial cells.

8 o reduced bacterial internalization by renal tubular epithelial cells.

9 ous functional parameters in endothelial and tubular epithelial cells.

10 e expressed in nuclei of proximal and distal tubular epithelial cells.

11 The smallest crystals were endocytosed by tubular epithelial cells.

12 n-induced apoptosis of immortalized proximal tubular epithelial cells.

13 d larval survival and proliferation of renal tubular epithelial cells.

14 tection with persisting reduced apoptosis of tubular epithelial cells.

15 and sonic hedgehog ligands) are expressed in tubular epithelial cells.

16 appaB/NF-kappaB activation in human proximal tubular epithelial cells.

17 B-mediated cyclooxygenase-2 (COX-2) in renal tubular epithelial cells.

18 membrane transporters on the luminal side of tubular epithelial cells.

19 BK polyomavirus in primary cultures of renal tubular epithelial cells.

20 stress-responsive protective gene in kidney tubular epithelial cells.

21 ass transmembrane protein expressed in renal tubular epithelial cells.

22 the effect of complement on the phenotype of tubular epithelial cells.

23 a redox-dependent activation of Akt in renal tubular epithelial cells.

24 xidized lipoproteins, expressed by apoptotic tubular epithelial cells.

25 e actin and expression of S100A4 in proximal tubular epithelial cells.

26 s well as a microfluorimetry study of kidney tubular epithelial cells.

27 Nase I and EndoG mediate cisplatin injury to tubular epithelial cells.

28 ction of laminin-beta1 synthesis in proximal tubular epithelial cells.

29 ury by enhancing autophagy in renal proximal tubular epithelial cells.

30 plex with ILK at the focal adhesion sites of tubular epithelial cells.

31 nd RelB, which were predominantly located in tubular epithelial cells.

32 y and downregulated E-cadherin expression in tubular epithelial cells.

33 is followed by regeneration of damaged renal tubular epithelial cells.

34 regenerating tubules are derived from renal tubular epithelial cells.

35 aspase 3 expression, present mostly on renal tubular epithelial cells.

36 gainst the in vitro hypoxia injury of kidney tubular epithelial cells.

37 cing factor (AIF) in cisplatin-treated renal tubular epithelial cells.

38 specifically and permanently in mature renal tubular epithelial cells.

39 crystal-induced cell death in primary human tubular epithelial cells.

40 Sirt5 was highly expressed in proximal tubular epithelial cells.

41 ty acid oxidation in the Sirt5(-/-) proximal tubular epithelial cells.

42 expression and promotes cell cycle entry of tubular epithelial cells.

43 time-dependently alters CLDN-2 expression in tubular epithelial cells.

44 A induced Nupr1 expression in cultured human tubular epithelial cells.

45 ct of oxidative DNA damage) in podocytes and tubular epithelial cells.

46 ng on glomerular endothelial cells and renal tubular epithelial cells.

47 , pre-, and pri-miR-214 than normal proximal tubular epithelial cells.

48 hi homologue 1 (Msi1), which is expressed in tubular epithelial cells.

49 titutively expressed by human renal proximal tubular epithelial cells.

50 nterstitium and in TNFalpha-treated proximal tubular epithelial cells.

51 ed in proximity to the polyomavirus-infected tubular epithelial cells.

52 uced alterations in these levels in proximal tubular epithelial cells.

53 nd shRNA knockdown strains in renal proximal tubular epithelial cells.

54 the sustained in-vivo modification of renal tubular epithelial cells.

55 ansmembrane TNF-alpha in cultured CD4- renal tubular epithelial cells, 293T cells, and HeLa cells ena

56 In transfected tubular epithelial cells, 4-PBA did not improve maturati

57 beta-catenin, predominantly in podocytes and tubular epithelial cells, accompanied renal injury; pari

58 c miR-24 enrichment in renal endothelial and tubular epithelial cells after I/R induction.

59 nd downstream Src activation both in primary tubular epithelial cells after in vitro stimulation with

60 ound to be induced rapidly in human proximal tubular epithelial cells after TGF-beta1 treatment.

61 results suggest that netrin-1 protects renal tubular epithelial cells against ischemia reperfusion-in

62 wever, Mif gene deletion restricted to renal tubular epithelial cells aggravated these effects.

63 pses between HIV-harboring T cells and renal tubular epithelial cells, allowing viral uptake and gene

64 overexpression of DNase I in cultured mouse tubular epithelial cells also induced EndoG.

65 along endothelial cells and inside proximal tubular epithelial cells also.

66 ithelial-specific genetic ablation of Myc in tubular epithelial cells ameliorated fibrosis and restor

67 nuria caused a decrease in the proportion of tubular epithelial cells and an increase in the proporti

68 7-deficient mice exhibited less apoptosis of tubular epithelial cells and better renal function than

69 t natural killer (NK) cells are cytotoxic to tubular epithelial cells and contribute to acute kidney

70 important because it typically damages renal tubular epithelial cells and glomerular cells and is the

71 e kidneys was observed primarily in cortical tubular epithelial cells and in correlation with the pro

72 uction of proinflammatory mediators by renal tubular epithelial cells and inflammatory cells (eg, mon

73 atory responses through acting on both renal tubular epithelial cells and inflammatory cells and by i

74 CYP3A5 protein expression was detected in tubular epithelial cells and inflammatory cells within t

75 Cell proliferation of both tubular epithelial cells and interstitial cells is reduc

76 MP-activated protein kinase (AMPK) in kidney tubular epithelial cells and interstitial fibroblasts.

77 duced inflammatory mediators from both renal tubular epithelial cells and macrophages after hypoxia/r

78 at Dragon may enhance BMP signaling in renal tubular epithelial cells and maintain normal renal physi

79 expression and H3K79 dimethylation in renal tubular epithelial cells and myofibroblasts in a murine

80 and p21 expression in human kidney 2 (HK-2) tubular epithelial cells and normal rat kidney-49 fibrob

81 ted with fluorescently tagged HIV with renal tubular epithelial cells and observed efficient virus tr

82 TMIGD1 is expressed in renal tubular epithelial cells and promotes cell survival.

83 bules occurs primarily from proliferation of tubular epithelial cells and resident renal-specific ste

84 ecovery and repair involves proliferation of tubular epithelial cells and stem cell populations and t

85 d multicellular tubulogenesis in mouse renal tubular epithelial cells and that these morphogenic effe

86 UUO), HDAC8 was primarily expressed in renal tubular epithelial cells and time-dependently upregulate

87 to TrkA phosphorylation in mesangial cells, tubular epithelial cells, and podocytes but not in glome

88 activate transforming growth factor-beta1 in tubular epithelial cells, and this process occurred in a

89 ice developed mesangial matrix expansion and tubular epithelial cell apoptosis in association with in

90 s and macrophages, chemokine expression, and tubular epithelial cell apoptosis in kidney.

91 Proximal tubular epithelial cells are highly energy demanding.

92 l cycle dysregulation and apoptosis of renal tubular epithelial cells are important components of the

93 Despite that tubular epithelial cells are the major sites of active v

94 f epithelial-mesenchymal transition, whereby tubular epithelial cells are transformed into activated

95 primary site of damage during AKI, proximal tubular epithelial cells, are highly metabolically activ

96 1 treatment also reduced the number of renal tubular epithelial cells arrested at the G2/M phase of t

97 layed calcium oxalate crystals inside distal tubular epithelial cells associated with mitochondrial c

98 proliferating cell nuclear antigen-positive tubular epithelial cells at 24 hours after the ischemia-

99 These findings demonstrate that tubular epithelial cells at the perimeter of the macula

100 During proteinuria, renal tubular epithelial cells become exposed to ultrafiltrate

101 In tubular epithelial cells, both norepinephrine and CGRP i

102 tin expression in TSC2(+/-) primary proximal tubular epithelial cells; both inhibition of Akt and inh

103 injury (AKI) with adaptive proliferation of tubular epithelial cells, but repair can also lead to fi

104 ates tight junction-associated activities in tubular epithelial cells, but the function of DbpA in me

105 nin-beta1 synthesis in murine renal proximal tubular epithelial cells by 30 mmol/l glucose (high gluc

106 r 2 (TNFR2) is strongly upregulated on renal tubular epithelial cells by acute cell-mediated rejectio

107 Damage to renal tubular epithelial cells by genetic, environmental, or b

108 trix protein laminin-beta1 in renal proximal tubular epithelial cells by stimulation of initiation ph

109 VHL led to dysplastic hyperproliferation of tubular epithelial cells, confirming the procarcinogenic

110 ubulointerstitium; dh404 markedly suppressed tubular epithelial cell damage in the renal interstitium

111 reated with unilateral renal IRI, persistent tubular epithelial cell damage was determined in the IRI

112 -1R(+) or CD68(+)) that induced apoptosis of tubular epithelial cells, damaging the kidney.

113 ntin, which can activate NK cells to mediate tubular epithelial cell death in vitro, was highly expre

114 rized by uncontrolled renal inflammation and tubular epithelial cell death.

115 In renal tubular epithelial cells, decreased Smad3 levels were ob

116 ository of the RBPome and proteome in kidney tubular epithelial cells, derived from our findings, is

117 Ca(2+) ion channels, respectively, result in tubular epithelial cell-derived renal cysts.

118 Mice lacking Cdc42 specifically in kidney tubular epithelial cells died of renal failure within we

119 However, podocytes and renal tubular epithelial cells do not express CD4 receptors, a

120 sed expression of 6-O-sulfated HS domains in tubular epithelial cells during chronic rejection as com

121 olves numerous different cell types, such as tubular epithelial cells, endothelial cells, and podocyt

122 ndMT, resulted in increased Myc abundance in tubular epithelial cells, enhanced glycolysis, and suppr

123 suppression of UNC5B expression in cultured tubular epithelial cells exacerbated cisplatin-induced c

124 ion, whereas IL-22 receptor was expressed by tubular epithelial cells exclusively.

125 Tubular epithelial cells exposed to serum proteins adopt

126 Nearly all renal tubular epithelial cells express insulin receptor.

127 induced tubulointerstitial injury, with some tubular epithelial cells expressing alpha-smooth muscle

128 Tubular epithelial cell expression of SPI-6 blocks granz

129 Studies have shown that podocytes and renal tubular epithelial cells from patients with HIV-associat

130 astructure of fibroblasts and renal proximal tubular epithelial cells from patients with three clinic

131 Renal tubular epithelial cells from SIRP-alpha(mut) mice produ

132 ression of PSF-TFE3 in normal renal proximal tubular epithelial cells from where such tumors originat

133 core role for miR-192 in mediating proximal tubular epithelial cell G2/M arrest after toxic injury b

134 served increased apoptosis in renal proximal tubular epithelial cells, greater expression of LC3-II/L

135 In addition, Nlrp3KO tubular epithelial cells had an increased repair respons

136 In a separate arm, renal tubular epithelial cells (HK-2) were directly stimulated

137 Human proximal tubular epithelial cells (HK-2) were examined after incu

138 In cultured human kidney tubular epithelial cells (HK-2), TGF-beta1 treatment ind

139 an hepatic epithelial cells (L-02) and human tubular epithelial cells (HK-2).

140 Human proximal tubular epithelial cells (HK2 cells) undergo EMT in resp

141 Alu-containing (SnoN) expression in proximal tubular epithelial cells (HKC-8) but not in glomerular m

142 -1-induced RANTES expression in human kidney tubular epithelial cells (HKC-8).

143 acid are linked to growth arrest of proximal tubular epithelial cells; however, the underlying mechan

144 We show that primary human proximal tubular epithelial cells (HPTECs) possess characteristic

145 kidneys or oxidant stress in human proximal tubular epithelial cells (HPTECs), KIM-1 expression incr

146 s BKV entry pathways in human renal proximal tubular epithelial cells (HRPTEC) and, correspondently,

147 Since human renal proximal tubular epithelial cells (HRPTEC) represent a main natur

148 ithelial cells (HiBEC), human renal proximal tubular epithelial cells, human bronchial epithelial cel

149 ling pathways, mediates Ang II-induced renal tubular epithelial cell hypertrophy.

150 RNA and protein expression in human proximal tubular epithelial cells in a time-dependent fashion, an

151 und that Nod1 and Nod2 were present in renal tubular epithelial cells in both mouse and human kidneys

152 VEGF-positive cells were observed mainly in tubular epithelial cells in CO-treated, but not air-expo

153 Mice or renal proximal tubular epithelial cells in culture were exposed to cisp

154 e tuberin/mTOR pathway promotes apoptosis of tubular epithelial cells in diabetes, mediated in part b

155 The proliferation of mouse proximal tubular epithelial cells in ex vivo culture depends on m

156 in-like protein that is upregulated in renal tubular epithelial cells in HIVAN.

157 gnificantly decreased frequency of apoptotic tubular epithelial cells in IFNAR-deficient mice, as com

158 VEGFA is also expressed in tubular epithelial cells in kidney; however, its physiol

159 Tubular epithelial cells in normal kidney organ cultures

160 Renal tubular epithelial cells in S-phase were scored as femal

161 ular elongation and shape maintenance of two tubular epithelial cells in the C. elegans excretory sys

162 ized predominantly to the apical surfaces of tubular epithelial cells in the thick ascending limbs, d

163 is by using Madin-Darby Canine Kidney (MDCK) tubular epithelial cells in two- or three-dimensional (2

164 adhesion molecules, CD44 and annexin II, in tubular epithelial cells in vitro and in vivo, and treat

165 re, inhibition of Crry expressed by proximal tubular epithelial cells in vitro resulted in alternativ

166 In human proximal tubular epithelial cells in vitro, PAR2 stimulation with

167 toxic effects on renal endothelial cells and tubular epithelial cells in vitro.

168 many epithelial cell types, including renal tubular epithelial cells, in which they are felt to part

169 e role of RNA-protein interactions in kidney tubular epithelial cells, including the response of thes

170 catenin in the cytoplasm and nuclei of renal tubular epithelial cells, indicating activation of the c

171 Tubular epithelial cells induce significant CD8+ T-cell

172 Tubular epithelial cell-induced CD8 degranulation and CD

173 plasmin (20 microg/ml) to cultures of murine tubular epithelial cells initiated ERK phosphorylation w

174 Meprin A plays an important role in tubular epithelial cell injury during acute kidney injur

175 or of obstruction-induced renal fibrosis and tubular epithelial cell injury independent of TGF-beta1

176 affected patients are secondary to extensive tubular epithelial cell injury induced by the lytic repl

177 uch growth arrest to fibrosis after proximal tubular epithelial cell injury, this mechanism may have

178 tigen was detected in less than 5% of VSMCs, tubular epithelial cells, interstitial endothelium, inte

179 Oxidative damage to renal tubular epithelial cells is a fundamental pathogenic mec

180 elatively unknown, despite that apoptosis of tubular epithelial cells is commonly observed in human r

181 The dysfunction and apoptosis/necrosis of tubular epithelial cells is of key importance for the pa

182 complex, localizes to primary cilia of renal tubular epithelial cells, is required for ciliogenesis,

183 uring kidney morphogenesis and repair, renal tubular epithelial cells lacking the transmembrane recep

184 In human renal tubular epithelial cell line (HK-2), VAN induced p53 acc

185 line (LLC-EZ) using the pig kidney proximal tubular epithelial cell line (LLC-PK1), which constituti

186 n microarray studies that used a novel renal tubular epithelial cell line from a patient with HIVAN,

187 result of oxidative stress; in the proximal tubular epithelial cell line HK-2, TINag expression and

188 yzed this region in the human renal proximal tubular epithelial cell line HK-2.

189 In MDCK, a kidney tubular epithelial cell line, cells, low concentrations

190 study conducted on the human renal proximal tubular epithelial cell line, RPTEC/TERT1, treated with

191 mation was studied in vitro using a proximal tubular epithelial cell line.

192 ablished conditionally immortalized proximal-tubular epithelial cell lines (ciPTECs) from three patie

193 macula densa, the observation was made that tubular epithelial cells located near the macula densa a

194 tated NLRP3 inflammasome activation in renal tubular epithelial cells, macrophages, and dendritic cel

195 receptor on the surface of injured proximal tubular epithelial cells, mediating phagocytosis of apop

196 he expression of clusterin in renal proximal tubular epithelial cells obtained from patients with nep

197 reased expression of IL-36alpha in the renal tubular epithelial cells of a mouse model of unilateral

198 Apoptosis was also detected in the tubular epithelial cells of CP-treated mice using immuno

199 iopoietin-2 expression markedly increased in tubular epithelial cells of fibrotic kidneys but decreas

200 The tubular epithelial cells of ICGN mice showed a decrease

201 be overexpressed in the proximal and distal tubular epithelial cells of murine and human kidneys aft

202 ripts for the IL-27RA and the IL-17RA in the tubular epithelial cells of patients with renal fibrosis

203 nstrated that these factors are expressed in tubular epithelial cells of postischemic kidneys.

204 es, BK virus (BKV) replication occurs in the tubular epithelial cells of the kidney, causing nephropa

205 a low level of regenerative competence, the tubular epithelial cells of the nephrons can proliferate

206 d that the absence of C3aR and C5aR on renal tubular epithelial cells or circulating leukocytes atten

207 BMDC contributed to the renal tubular epithelial cell population, although most (90%)

208 During kidney organogenesis, tubular epithelial cells proliferate until a functional

209 or-independent mechanism to facilitate renal tubular epithelial cell proliferation and renal tubular

210 he intracellular mechanisms underlying renal tubular epithelial cell proliferation and tubular repair

211 n of plasma creatinine correlating with less tubular epithelial cell proliferation compared to the yo

212 Similar reductions in renal tubular epithelial cell proliferation were observed foll

213 either globally or conditionally in proximal tubular epithelial cells, protected mice from the develo

214 al tubular epithelial cellcaused by proximal tubular epithelial cell (PTC) apoptosis.

215 s and determine its effect on renal proximal tubular epithelial cell (PTC) function, because this is

216 phenotypic modulation of the renal proximal tubular epithelial cell (PTC).

217 Factor H dose-dependently bound to proximal tubular epithelial cells (PTEC) in vitro.

218 rotic target cells by viable kidney proximal tubular epithelial cells (PTEC) modulates the activity o

219 Impaired albumin reabsorption by proximal tubular epithelial cells (PTECs) has been highlighted in

220 Mouse proximal tubular epithelial cells (PTECs) in culture were then ex

221 totic target cells by viable kidney proximal tubular epithelial cells (PTECs) inhibits the proliferat

222 ial-mesenchymal transition (EMT) of proximal tubular epithelial cells (PTECs) into myofibroblasts con

223 Yet, the responses of proximal tubular epithelial cells (PTECs) to fluid flow remain un

224 ltured MAIT cells and human primary proximal tubular epithelial cells (PTECs) under hypoxic (1% oxyge

225 Injury of proximal tubular epithelial cells rapidly and strongly induced Nu

226 We used human renal proximal tubular epithelial cells, rat kidney transplants, and HO

227 In addition to tubular epithelial cells, recent studies indicate that e

228 of endogenous AGS3 mRNA and protein in renal tubular epithelial cells reduced cell proliferation in v

229 In this study, we found that dying tubular epithelial cells released histones into the extr

230 otein 13 (TRIP13) is a critical modulator of tubular epithelial cell repair following ischemia-reperf

231 nd Hmox1 in centrilobular hepatocytes and in tubular epithelial cells, respectively.

232 ey injury induces cell cycle arrest in renal tubular epithelial cells, resulting in the secretion of

233 ate proinflammatory events in renal proximal tubular epithelial cells (RPTEC) via interaction with CD

234 Dysregulated apoptosis of renal tubular epithelial cells (RTEC) is an important componen

235 Here, using renal tubular epithelial cells (RTECs) derived from FAT10(-/-)

236 We hypothesized that renal tubular epithelial cells (RTECs) isolated from hibernati

237 Renal tubular epithelial cells (RTECs) perform the essential f

238 otoxicity, and inflammatory insults to renal tubular epithelial cells (RTECs), resulting in the onset

239 hagosome and autolysosome formation in renal tubular epithelial cells (RTECs).

240 Both glomerular and tubular epithelial cells showed enhanced expression of p

241 Tubular epithelial cells showed strong production of per

242 Studies in kidney-proximal tubular epithelial cells showed that SNP abrogated high

243 Notably, tubular epithelial cell-specific overexpression of IL-17

244 In human proximal tubular epithelial cells, stimulation by fluvoxamine or

245 and EMT through the NF-kappaB pathway in the tubular epithelial cells, suggesting a novel role for th

246 Renal tubular epithelial cells synthesize laminin (LN)5 during

247 accumulation, activation, and Mphi-mediated tubular epithelial cell (TEC) apoptosis during unilatera

248 h subclinical rejection, suggesting that the tubular epithelial cell (TEC) expression of this protein

249 Clear cell renal cell carcinoma (ccRCC), a tubular epithelial cell (TEC) malignancy, frequently sec

250 chemic renal injury is often reversible, and tubular epithelial cell (TEC) proliferation is a hallmar

251 ed that miR-21 is expressed in proliferating tubular epithelial cells (TEC) and up-regulated by both

252 TNFR) superfamily, is induced in human renal tubular epithelial cells (TEC) in response to injury.

253 Previous studies revealed that tubular epithelial cells (TEC) show a limited response t

254 tor (CSF)-1 and its receptor CSF-1R on renal tubular epithelial cells (TEC) will promote proliferatio

255 IL-34 was generated by tubular epithelial cells (TECs) and promoted Mo-mediated

256 To elucidate the mechanisms by which renal tubular epithelial cells (TECs) control the complement s

257 ation, and activation, is upregulated in the tubular epithelial cells (TECs) during kidney inflammati

258 ceptor superfamily, is up-regulated in human tubular epithelial cells (TECs) during renal injury, but

259 show that activation of the Notch pathway in tubular epithelial cells (TECs) in patients and in mouse

260 NK) cell-mediated cytotoxicity against renal tubular epithelial cells (TECs) plays a crucial role dur

261 We hypothesize that human renal tubular epithelial cells (TECs) trigger selective prolif

262 NLRP3 expression in renal tubular epithelial cells (TECs) was found to be an impor

263 survival and proliferation, is expressed by tubular epithelial cells (TECs), and binds to the cFMS r

264 pithelial-to-mesenchymal transition (EMT) of tubular epithelial cells (TECs).

265 In proximal tubular epithelial cells, TGF-beta1 treatment causes a d

266 VTEA enabled us to discover a population of tubular epithelial cells that expresses CD11C, a marker

267 Snail1 reactivation induces a partial EMT in tubular epithelial cells that, without directly contribu

268 Here macrophages, growth-arrested tubular epithelial cells, the endothelium, and surroundi

269 t, FBP1 antagonizes glycolytic flux in renal tubular epithelial cells, the presumptive ccRCC cell of

270 sitive cells relative to interstitial space, tubular epithelial cells, the tubular basement membrane

271 -1 also increased albumin uptake by proximal tubular epithelial cells through the PI3K and ERK pathwa

272 Exposure of renal proximal tubular epithelial cells to 10 mum cadmium demonstrated

273 In vitro exposure of human renal proximal tubular epithelial cells to C5a led to altered mitochond

274 Exposure of proximal tubular epithelial cells to high glucose causes a rapid

275 Exposure of proximal tubular epithelial cells to high glucose contributes to

276 beta1 integrin was required for renal tubular epithelial cells to mediate GDNF- and FGF-depend

277 IP13 increased the susceptibility of damaged tubular epithelial cells to progress towards apoptotic c

278 peroxisomal fatty acid oxidation in proximal tubular epithelial cells to protect against injury in AK

279 ogressive tubulointerstitial fibrosis, renal tubular epithelial cells transform into alpha-smooth mus

280 In vascular smooth muscle cells and renal tubular epithelial cells, treatment with thrombospondin-

281 th muscle actin and fibronectin induction in tubular epithelial cells, underscoring its ability to bl

282 reteral obstruction model of renal fibrosis, tubular epithelial cells upregulated the chemokine CXCL1

283 st that IL-18 induces profibrotic changes in tubular epithelial cells via increased TLR4 expression/s

284 acid led to profound G2/M arrest in proximal tubular epithelial cells via p53-mediated inactivation o

285 etion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC1 defi

286 ed protein p62/SQSTM1 in cystinotic proximal tubular epithelial cells, we performed a high-throughput

287 TAM expression and shedding by tubular epithelial cells were investigated by PCR and en

288 Murine renal tubular epithelial cells were studied in response to in

289 To test the role of HO-1, renal proximal tubular epithelial cells were treated with HO-1 small in

290 Primary mouse tubular epithelial cells were treated with methylglyoxal

291 many epithelial cell types, including renal tubular epithelial cells, where they participate in flow

292 leomorphic nuclei in the proximal and distal tubular epithelial cells, which was associated with inte

293 ssion and activity at 24 h in renal proximal tubular epithelial cells, which was inhibited by sodium

294 e infected immortalized and primary proximal tubular epithelial cells with adenovirus to express eith

295 in type 1 diabetes and treatment of proximal tubular epithelial cells with high glucose leads to phos

296 with these findings, treating human proximal tubular epithelial cells with PAR2-AP induced Smad2/3 ph

297 dneys undergoing ACR represent proliferating tubular epithelial cells with TNFR2-induced stem cell ma

298 of vascular smooth muscle cells (VSMCs) and tubular epithelial cells, with a median positivity of 20

299 ptor type 1 (TbetaR1) kinase specifically in tubular epithelial cells, with expression restricted by

300 nduced a biphasic activation of ILK in renal tubular epithelial cells, with rapid activation starting